Gut microbial metabolites as a convergence point between autoimmunity and solid tumors

TL;DR

This paper explores how gut microbial metabolites influence both autoimmunity and cancer, highlighting their role in immune regulation and disease progression.

Contribution

The paper provides a comprehensive review of the emerging link between gut microbial metabolites and cancer immunoediting.

Findings

Gut microbial metabolites modulate immune responses through Tregs and Th17 cells.

Dysbiosis is associated with autoimmune disorders and cancer development.

Microbial metabolites may promote or suppress cancer via inflammation and immunosuppression.

Abstract

The human gut microbiome, a diverse community of trillions of microorganisms, is essential for controlling numerous bodily functions, such as metabolism, immune response, and epithelial barrier integrity. The gut microbiota comprises bacteria, viruses, fungi, and other microorganisms that affect human health, metabolic pathways, and immune responses. Dysbiosis, or the imbalance of gut microbial composition, has been linked to the pathogenesis of several ailments, including cardiovascular conditions, gastrointestinal conditions, allergies, obesity, autoimmune disorders, and tumors. The interaction between gut microbes and immune responses, mainly through Tregs cells and Th17 cells, underscores the microbiome’s function in immune regulation. Furthermore, gut microbial metabolites act as signaling molecules and substrates for metabolic processes, impacting autoimmune disorders and cancer development. Recent research highlights the microbiome’s potential role in cancer immunoediting, where gut microbial metabolites may either promote or suppress cancer progression by modulating inflammation and immunosuppression. This review delves into the critical functions of the gut microbiome, its influence on autoimmune disorders, and the emerging connection between gut microbial metabolites and cancer immunoediting, offering new insights into their impact on human health and disease.

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